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Biomedical subjects

A D Durnev

Publications and source records attributed to A D Durnev.

At least 37 records · Page 2Linked to original sources
PubMed2000

Effects of beta-carotene and aspartame on clustogenic activity of cyclophosphamide and dioxidine in mice.

Antimutagenic effects of combination of aspartame (0.4 and 4 mg/kg) and beta-carotene (0.15-15 mg/kg) were studied by estimation of chromosome aberrations in bone marrow cells of C57Bl/6 mice. Single and 5-day treatment with this combination decreased the clastogenic effects of dioxidine and cyclophosphamide and produced a more potent and universal antimutagenic effect than its constituents.

Animals↗
PubMed1999

Verapamil contributes to the clastogenic effects of acrylamide, cyclophosphamide, and dioxidine on somatic cells of BALB/C and C57BL/6 mice.

The chromosome aberration assay of metaphase bone marrow cells was used to study the clastogenic effects of acrylamide, cyclophosphamide, dioxidine, and their combinations with Verapamil (a calcium antagonist) in male BALB/C and C57BL/6 mice. Verapamil gavage at single (5 mg/kg) and repeated doses (2.5 and 5 mg/kg five times at 24-h intervals) significantly enhanced the clastogenic activity of acrylamide (50 and 100 mg/kg intraperitoneally) in BALB/C mice; in C57BL/6 mice, this effect was only observed when they received Verapamil at doses of 2.5 mg/kg for 5 days. Verapamil administered repeatedly (2.5-10 mg, gavage) significantly increased the clastogenic activity of cyclophosphamide (10 mg/kg intraperitoneally) in C57BL/6 mice. In BALB/C mice, this effect of Verapamil was only observed at a dose of 10 mg/kg (gavage). When injected intraperitoneally at a single dose of 0.1-0.4 mg/kg, Verapamil significantly enhanced the clastogenic activity of cyclophosphamide in mice of both strains. This calcium antagonist produced identical effects when administered to BALB/C mice intraperitoneally (2.5 and 5 mg/kg) and by gavage (5 mg/kg) and to C57BL/6 mice intraperitoneally (5 and 10 mg/kg) and by gavage (2.5 mg/kg). Repeated administration of Verapamil (at all doses tested) promoted the clastogenic effect of dioxidine (100 mg/kg intraperitoneally) on C57BL/6 mice, having no such influence on BALB/C mice. These results demonstrate the co-clastogenic activity of Verapamil in mice and suggest that its specific manifestations depend on the dose, method, and route of drug administration and the genotype of test animals.

Acrylamide↗
PubMed1999

[Spontaneous death of mononuclear cells, obtained from health donors and patients with systemic lupus erythematosus].

Unstimulated human peripheral blood mononuclear cells (MNC) underwent death during incubation in vitro. According to morphological criteria the type of death was identified as apoptosis. There was a good correlation between a fraction of apoptotic cells qualified morphologically, and fraction of "apoptotic" comets. The use of DNA-comets for studying the spontaneous death in vitro of MNC from patients with systemic lupus erythematosus (SLE) showed that 24 h after isolation cells from SLE patients demonstrated a higher level of apoptosis than MNC from normal donors. It is likely that the increased apoptosis of SLE-MNC in vitro may reflect changes occurring in those cells in vivo which are bound with pathogenesis of disease. In this context the comet assay may be promising in diagnostics and monitoring of therapeutic treatments.

Apoptosis↗
PubMed1998

The influence of two carotenoid food dyes on clastogenic activities of cyclophosphamide and dioxidine in mice.

The influence of the food dyes E160e (beta-apo-8'-carotenal in an oil suspension) and E160a (beta-carotene in an oil suspension) on clastogenic effects of cyclophosphamide (CP) and dioxidine (DN) was investigated. Chromosome damage in the bone marrow of C57BL/6 mice was reported. The following protocols were used: (1) simultaneous single administration of the dye and the mutagen and the subsequent animal sacrifice within 24 hr; (2) a 4-day pretreatment with the dye (daily administrations) followed with simultaneous injection of the dye and the mutagen on the 5th day 24 hr before sacrifice; (3) daily co-administration of the dye and the mutagen for 5 days with sacrifice 6 hr after the last administration. CP at a dose of 30 mg/kg and DN at 300 mg/kg were injected intraperitoneally; the dyes at doses of 0.5, 5 and 50 mg/kg were given orally. Under all the protocols applied, E160e at a dose of 50 mg/kg caused a significant reduction of both DN and CP effects. At 5 mg/kg this dye reduced the effects of the mutagens only under the pretreatment regimen. Pretreatment with E160a at doses of 5 and 50 mg/kg resulted in a meaningful reduction of the DN effect. Under the combined treatment with mutagens this dye reduced both CP and DN effects.

Animals↗
PubMed1997

[Mutagens and antimutagens in food products].

Probable pathways of food contamination with environmental chemical mutagens and factors responsible for the formation of mutagens in food during cooking are reviewed, and natural and synthetic food components with mutagenic properties are described. The data discussed provide evidence for the expediency of further analyzing mutagenicity of various food components and developing chemical analytical methods for their detection and identification. Antimutagenic compounds present in food are characterized. The adequacy of methods for estimating the activity of these compounds and perspectives for their use as antimutagenic chemopreventive agents are discussed. Emphasis is placed on the necessity of being extremely cautious in employing food antimutagens because of the probable inversion of their effects. Several examples are provided to demonstrate the possibility of reducing mutagenicity of prepared food by modifying food processing technology.

Animals↗
PubMed1997

[Mutagen-modifying effects of beta-carotene in vivo].

A chromosome aberration test on bone marrow cells of C57B1/6 mice showed that beta-carotene (BC) applied by oral administration as a E160a food dye (30% oil suspension) at doses of 0.5, 5, and 50 mg/kg simultaneously with cyclophosphamide (CPA) and dioxidine (DN) injected intraperitoneally for a period of 24 h did not modify their clastogenic effects. If the animals were pretreated with perorally administrated beta-carotene dye at doses of 5 and 50 mg/kg (corresponding to 1.5 and 15 mg/kg of BC) for 5 consecutive days, a statistically significant reduction in the clastogenic effect of the DN injected for 24 h but not the CPA was observed. In another set of experiments, E160a and clastogens were administered simultaneously for 5 consecutive days, and the animals were killed 6 h after the last treatment. In this case, BC at the dose of 0.15-15 mg/kg statistically significantly reduced the clastogenicity of DN at all doses used, and of CPA at doses of 1.5 and 15 mg/kg.

Animals↗
PubMed1997

[Effects of food carotenoid dyes E160a and E160e on clastogenic activity of cyclophosphamide and dioxidine in mice].

The action of the food dyes E160e (20% beta-apo-8'-carotinale in oily suspension) and E160e (20% beta-carotene in oily suspension) on the clastogenic effects of the indirect alkylating mutagen cyclophosphamide (CP) and the prooxidative mutagen dioxidine (D) was examined by the using the chromosomal aberrations tests on the bone marrow cells from C57B1/6 mice. E160e in a dose of 50 mg/kg caused a significant decrease in the count of aberrant cells damaged by D or CP. When given in a dose 5 mg/kg, the dye reduced the effects of these mutagens only during preadministration. Moreover, E160e in a dose of 0.5 mg/kg substantially lowered the clastogenic effect of D after its 5-day use in combination with the mutagen E160a. Pretreatment of the animals with E160a in doses of 5 und 50 mg/kg caused a significant reduction in the cytogenetic effect of D. When used in combination with the mutagens, this dye in doses of 5 and 50 mg/kg reduced the clastogenic action of CP, when given in doses of 0.5, 5, and 50 mg/kg, it decreased the count of cells damaged by D. In other variants of the experiment E160a was inactive.

Animals↗
PubMed1997

[Comparative study of DNA-repair ability of lymphocytes from systemic lupus erythematosus and rheumatoid arthritis patients].

Induction of DNA breaks with 4-NQO and their resynthesis in the cultivated lymphocytes of peripheral blood of 23 patients with systemic lupus erythematosus (SLE) and 12 patients with rheumatoid arthritis (RA) were studied by the method of hydroxyapatite column chromatography of cell lysates. The number of spontaneous DNA breaks was shown to increase in 48% of patients with SLE and in 42% of patients with RA, compared to that in the control. Inhibition of the repair process was observed in 35% of patients with SLE and in 17% of patients with RA. Complete repair of DNA breaks was observed in 67% of patients with RA and only in 26% of patients with SLE.

4-Nitroquinoline-1-oxide↗
PubMed1996

[Active forms of oxygen and pathogenesis of rheumatoid arthritis and systemic lupus erythematosus].

In this paper the authors underline the significance of studies into the body's free radical oxidation, analyze the involvement of free radical reactions in the maintenance of homeostasis. They indicate that free radical metabolic changes leading to oxidative stress play a role in the pathogenesis of many human diseases. Particular emphasis is laid on the contribution of active forms of oxygen (AFO) in the development of autoimmune diseases, including rheumatic diseases. The history of this problem is outlined. There are examples that confirm the enhancement of free radical processes and the inhibition of the antioxidative system in rheumatic arthritis (RA) and some other rheumatic diseases. The essential drugs used in the treatment of RA patients are demonstrated to also act due to the inhibited "respiratory outbreak" of phagocytes. The key point of the paper is the role of free radical reactions in the pathogenesis of systemic lupus erythematosus (SLE). There is evidence suggesting that there is a reduction in antioxidative defense and a rise in neutrophilic production of AFO in SLE patients. Consideration is also given to the possible participation of AFO in the formation of DNA antibodies, the effects of AFO on the immune system, atherogenesis in SLE. Taking into account a possible contribution of AFO in the pathogenesis of SLE, it is expedient to include antiradical agents into the multimodality therapy for this disease and promising to continue investigations in this field.

Arthritis, Rheumatoid↗
PubMed1995

[Corpuscular mutagenesis and its prevention].

The carcinogenic and mutagenic activity of dust containing chrysotile-asbestos and zeolites, as well as the role of active oxygen species in their cytotoxic and mutagenic actions are discussed. Superoxide dismutase (50 mg/ml) was demonstrated to prevent the mutagenic effects of chrysotile-asbestos and latex, catalase (20 mg/ml) to prevent the same of zeolites in experiments on cultured human whole blood. The intraperitoneal administration of dusts of chrysotile-asbestos and zeolites in a dose of 50 mg/kg to C57B1/6 mice was found to elevate the count of cells with chromosomal aberrations in the peritoneal liquid and bone marrow cells of mice, which was dependent on dust exposure time. It was revealed that ascorbic acid, rutin, chemically modified flavonoid of Scutellaria Baicalensis Georgy, drugs such as bemitil and thomersol in the broad range of concentrations (10(-7)-10(-3) M) decreased or completely reduced the clustogenic action of zeolites and chrysotile-asbestos on cultured human whole blood. The ability of bemitil (1.8-19 mg/kg) rather than the others to prevent the mutagenic effect of chrysotile-asbestos was confirmed by the method of recording chromosomal aberrations in the cells of peritoneal liquid and bone marrow in mice. The findings suggest that the mutagenic effects of the corpuscular xenobiotics under study are mediated by active oxygen species and that the use of the models in vitro and in vivo is adequate for investigations into corpuscular mutagenesis. Based on their own data and literature data, the authors have defined possible lines of further research of corpuscular mutagenesis.

Adjuvants, Immunologic↗
PubMed1995

[Vitamin A and enzyme systems of metabolic activation of genotoxic compounds].

The study was undertaken to study the effects of N-nitrosodimethylamine (NDMA) on the formation of single-strand DNA breaks and gamma-glutamyltransferase-positive knots, the status of the enzymatic systems involved in NDMA metabolism and some other biochemical parameters when rats were on retinol-deficient diets and when they were given excessive vitamin A. The action of retinol on NDMA effects were analyzed by evaluating the activity of glutathione-S-transferase (EC 2.5.1.18), glutathione-reductase (EC 1.2.1.1), aldehyde-dehydrogenase and aldehyde-oxidase (EC 1.2.1.3 and EC 1.2.3.1, respectively), p-450 reductase NADPH cytochrome (EC 1.6.2.4), the demethylase and hydroxylase activities, levels of malonic dialdehyde and the rate of ascorbate-dependent lipid peroxidation, the contents of proteins, phospholipids, cysteine, redox glutathione, glucuronides, sulfates. The level of vitamin A in the animals was found to substantially affect the magnitude of the genotoxic action of NDMA. The supplementary administration of vitamin A reduced the effect of the carcinogen. The mechanism of protective action of retinol was largely explained by the mediated activity of cytochrome-P-450 and glutathione-dependent systems involved in the biotransformation of NDMA. Based on the data available in the literature and their own data, the authors analyzed the effects of retinol on the metabolism of genotoxicants and described possible mechanisms of its antimutagenic and anticarcinogenic action. It is concluded that the effective protection of the body from unfavourable environmental influences may be provided only by supplementary (more than the optimum) intake of vitamin A against the background of a damaging factor.

Animals↗